Calpain A controls mitotic synchrony in the Drosophila blastoderm embryo

- Calpain A loss-of-function results in mitotic progression defects during embryogenesis.
- Calpain A protein relocates from the cortex to spindle microtubules during mitosis.
- Cyclin B is a Calpain A target.
- A calcium wave activates Calpain A to control synchronized mitotic divisions.

The beautiful mitotic waves that characterize nuclear divisions in the early Drosophila embryo have been the subject of intense research to identify the elements that control mitosis. Calcium waves in phase with mitotic waves suggest that calcium signals control this synchronized pattern of nuclear divisions. However, protein targets that would translate these signals into mitotic control have not been described. Here we investigate the role of the calcium-dependent protease Calpain A in mitosis. We show that impaired Calpain A function results in loss of mitotic synchrony and ultimately halted embryonic development. The presence of defective microtubules and chromosomal architecture at the mitotic spindle during metaphase and anaphase and perturbed levels of Cyclin B indicate that Calpain A is required for the metaphase-to-anaphase transition. Our results suggest that Calpain A functions as part of a timing module in mitosis, at the interface between calcium signals and mitotic cycles of the Drosophila embryo.

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